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Fenofibrate is an antilipidemic drug that increases the activity of the lipoprotein lipase enzyme thus enhancing lipolysis, however, it may cause myopathy and rhabdomyolysis in humans. Coenzyme Q10 (CoQ10) is an endogenously synthesized compound that is found in most living cells and plays an important role in cellular metabolism. It acts as the electron carrier in the mitochondrial respiratory chain. This study aimed to elucidate FEN-induced skeletal muscle changes in rats and to evaluate CoQ10 efficacy in preventing or alleviating these changes. Forty adult male rats were divided equally into four groups: the negative control group that received saline, the positive control group that received CoQ10, the FEN-treated group received FEN, and the FEN+CoQ10 group, (received both FEN followed by CoQ10 daily for 4 weeks. Animals were sacrificed and blood samples were collected to assess creatine kinase (CK). Soleus muscle samples were taken and processed for light and electron microscopic studies. This study showed that FEN increased CK levels and induced inflammatory cellular infiltration and disorganization of muscular architecture with lost striations. FEN increased the percentage of degenerated collagen fibers, and immune expression of caspase 3. Ultrastructurally, it caused degeneration of myofibrils with distorted cell organelles. Treatment with CoQ10 could markedly ameliorate these FEN-induced structural changes and mostly regain the normal architecture of muscle fibers due to its antifibrotic and antiapoptotic effects. In conclusion, treatment with CoQ10 improved muscular structure by suppressing oxidative stress, attenuating inflammation, and inhibiting apoptosis.

Individuals with chronic renal failure (CRF) may have a variety of gastrointestinal (GI) problems, including dyspepsia, acid peptic disease, and bacterial overgrowth. We investigated gastrointestinal function in 11 uremic patients, seven of whom were on dialysis three times a week and four who were not on dialysis. Ten normal subjects were studied as controls. The nutritional status of the patients did not differ from that of the control subjects. Seven patients demonstrated abnormal GI endoscopic findings, although none was severe; they also had prolonged oral-cecal transit times but had no evidence of bacterial overgrowth, and all had normal numbers of lymphocyte subpopulations within the intestinal mucosa. The patients had significantly reduced activities of mucosal sucrase and maltase but not of lactase. In spite of the reductions in these enzymatic activities, carbohydrate malabsorption was not evident in the CRF group, probably because of the vast reserve of the small intestine. No differences were noted between the groups in the activities of several intestinal peptidases. From these data, we concluded that GI function is essentially normal in patients with CRF and postulate that this normality, which is in contrast to previous findings, is related to recent advances in the clinical management of uremic patients.

Methyltetrahydrofolic acid, formyltetrahydrofolic acid, folic acid and dihydrofolic acid were injected intravitreally into the eyes of chickens. No short-term or long-term signs of neurotoxicity were observed, even when doses 100–200 times those at which kainic acid produces clear neurotoxic effects were injected. The folic acid derivatives neither inhibited nor potentiated the neurotoxic effects. Thus no support is given to the suggestion that folic acid and its derivatives may act as kainic acid agonists or antagonists, even though the receptors involved in kainic acid-induced neurotoxicity appear to be of the kainic acid rather than quisqualic acid or N-methyl- d -aspartic acid type.

Lymphocyte subpopulations in the intestinal tissues of seven patients with acquired immunodeficiency syndrome (AIDS) or AIDS-related complex (ARC) were studied by immunohistologic technics at two different locations, the small bowel and the rectum. Intraepithelial and lamina propria lymphocyte subsets stained with monoclonal antibodies T11, T4, T8, and B1 were enumerated in the patients and different normal and patient control groups. Intraepithelial T11+ cells were decreased (P less than 0.05) in the small bowel of AIDS and ARC patients, primarily because of the near complete absence of T4+ lymphocytes. In the lamina propria of these patients, a depletion of T4+ cells (P less than 0.05), an increase in T8+ cells (P less than 0.05), and a reversal of the T4/T8 ratio were observed (e.g., the small bowel ratio was 0.1 +/- 0.02 vs. the normal ratio of 2.3 +/- 0.2 and the rectal ratios were 0.2 +/- 0.06 vs. normal 2.6 +/- 0.3). The T-lymphocytes in the intestine of AIDS and ARC patients did not express the receptor for interleukin-2 (IL-2). A near complete absence of T4+ lymphocytes was also seen in lymphoid follicles in the rectum. B1+ cells were not depleted. The reversal of the T4/T8 ratio, which is a hallmark of AIDS, occurs not only in the circulation but also in the gastrointestinal tissues of patients with AIDS and ARC.